Skip to main content

Advertisement

Fig. 1 | BMC Genomics

Fig. 1

From: Genome-wide mapping and profiling of γH2AX binding hotspots in response to different replication stress inducers

Fig. 1

Identification of damage sites caused by fork stalling reagents using γH2AX ChIP-seq. a Diagram illustrating ChIP-seq experimental design. Cells were grown in suspension and treated with indicated fork stalling agents (0.3 μM APH, 2 mM HU, or 200 μM MMS) for 24 h, followed by crosslinking and γH2AX ChIP. ChIP DNA was used for Illumina sequencing. b ChIP-seq replicates were internally Spearman Rank Correlation between ChIP-seq replicates. Bin size 1000 bp. c Genome browser tracks of ChIP-seq peaks under untreated and treated conditions. Approximately 1 Mb region is shown on chromosome 22 (left) and then a 12 kb region marked with the black box is amplified (right). ChIP-seq peaks are presented after normalizing to input. Numbers in parentheses indicate fold changes in γH2AX binding relative to input. Red boxes marked on the chromosome diagrams indicate approximate genomic positions of displayed histograms. d Venn Diagrams depicting overlaps of ChIP-seq peaks between untreated and treated samples. Overlaps between two samples are also illustrated. While overlap does exist between samples, a large portion of all data sets are unique

Back to article page